Obesity associated with worse oscillometry-defined small airway dysfunction in asthma

Key takeaways:

• Differences in small airway dysfunction persisted despite similarities in spirometry.
• Patients in one of the four patient clusters generally were older and female with obesity and more frequent exacerbations.

Patients with both asthma and obesity had significantly worse small airway dysfunction as defined by oscillometry compared with patients who did not have obesity, according to a study published in Annals of Allergy, Asthma & Immunology.

These outcomes were worse for these patients, based on oscillometry, despite comparable spirometry, asthma control, type 2 inflammation and exacerbation frequency, wrote Brian Lipworth, MD, head of the Scottish Centre for Respiratory Research, School of Medicine, University of Dundee, and Rory Chan, MBChB, PhD, principal investigator at the university.

The researchers classified the 188 adults with moderate to severe asthma in the study by BMI, including normal (18.5 kg/m²-24 kg/m²), overweight (25 kg/m²-29 kg/m²), obese (30 kg/m²-39 kg/m²) and morbidly obese (40 kg/m² and higher).

Compared with normal weight, obesity and morbid obesity were associated with significantly worse resistance between 5 Hz and 20 Hz (R5-R20), R5-R20 ratio, low-frequency resistance at 5 Hz (X5), area under the reactance curve (AX) and resonant frequency (Fres).

But across all groups, there were no significant differences in FEV₁, forced expiratory flow rate between 25% and 75% (FEF_25-75) of forced vital capacity (FVC), FEV₁/FVC ratio, peripheral blood eosinophils, fractional exhaled nitric oxide, total IgE, Asthma Control Questionnaire scores or severe exacerbation frequency.

In a pooled comparison, patients with obesity and morbid obesity had significantly worse oscillometry as resistance at 5 Hz, resistance at 20 Hz, R5-R20, X5, AX and Fres than the patients who did not have obesity or morbid obesity, although there were no differences in FEV₁, FEF_25-75, type 2 biomarkers, asthma symptom control or exacerbation frequency between the groups.

Using cluster analysis incorporating oscillometry, Lipworth and Chan identified four distinct asthma phenotypes:

• Cluster 1 (n = 72) included younger patients with obesity and preserved spirometry and oscillometry.
• Cluster 2 (n = 42) comprised older patients with obesity with normal spirometry but evidence of small airway dysfunction (SAD) on oscillometry.
• Cluster 3 (n = 38) encompassed older patients classified as overweight with impaired spirometry and airflow obstruction based on FEV₁/FVC but relatively well-preserved oscillometry.
• Cluster 4 (n = 31) included older women with obesity with combined spirometry and oscillometry impairment.

The fourth cluster also had significantly worse SAD based on FVC, R5-R20 ratio, R5-R20, AX, and severe exacerbation frequency requiring systemic corticosteroids compared with the other three clusters.

However, there were no differences in type 2 biomarkers between the groups.

Overall, the researchers said, these findings indicated significant differences in SAD measurements via oscillometry based on BMI despite relatively well-preserved spirometry in FEV₁ and FVC percentages.

With obesity conferring worse peripheral airway resistance and reactance measurements, the researchers said, an additive effect on lung mechanics due to obesity and severe asthma may be present.